ALUMINUM TOXICITY AND BINDING TO ESCHERICHIA-COLI
ALUMINUM TOXICITY AND BINDING TO ESCHERICHIA-COLI
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DOI：
10.1007/bf00245400
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发表时间：
1991-11-01
影响因子：
2.8
通讯作者：
POOLE, RK
中科院分区：
文献类型：
--
作者：
GUIDA, L;SAIDI, Z;POOLE, RK
本文研究了铝对大肠杆菌的毒性和结合作用。硝酸铝对生长的抑制作用明显依赖于pH，在pH为5.4的缓冲液中的生长对0.9 mM或2.25 mM的铝比在pH 6.6-6.8的生长更敏感。在用2-(N-吗啉)乙磺酸(MES)缓冲的培养基中，通过省略培养基中铁或使用指数相发酵剂可增强铝的毒性。原子吸收光谱分析表明，铝以胞内结合的形式存在，其K(M)为0.4 mm，结合容量为0.13摩尔(g干重)-1。相反，铝在细胞表面的结合发生在两个或更多的位置，并有协同作用的证据。将硝酸铝添加到缓冲较弱的细胞悬浮液中，可归因于金属阳离子将质子从细胞表面转移出来，从而导致介质酸化。结果表明，铝的毒性与pH相关的形态形成[Al(H2O)6(3+)可能是活性物种]和铝在介质中的络合作用有关。铝向细胞内结合部位的转运可能涉及Fe(III)的转运途径。
The toxicity and binding of aluminium to Escherichia coli has been studied. Inhibition of growth by aluminium nitrate was markedly dependent on pH; growth in medium buffered to pH 5.4 was more sensitive to 0.9 mM or 2.25 mM aluminium than was growth at pH 6.6 - 6.8. In medium buffered with 2-(N-morpholino)ethanesulphonic acid (MES), aluminium toxicity was enhanced by omission of iron from the medium or by use of exponential phase starter cultures. Analysis of bound aluminium by atomic absorption spectroscopy showed that aluminium was bound intracellularly at one type of site with a K(m) of 0.4 mM and a capacity of 0.13 mol (g dry wt)-1. In contrast, binding of aluminium at the cell surface occurred at two or more sites with evidence of cooperativity. Addition of aluminium nitrate to a weakly buffered cell suspension caused acidification of the medium attributable to displacement of protons from cell surfaces by metal cations. It is concluded that aluminium toxicity is related to pH-dependent speciation [with Al(H2O)6(3+) probably being the active species] and chelation of aluminium in the medium. Aluminium transport to intracellular binding sites may involve Fe(III) transport pathways.